Since females make stronger IFNα responses to HIV and have higher levels of immune activation for a given viral load than males4, we hypothesised that female fetuses also have higher levels of immune activation and are more susceptible than males to infection via IFNα-resistant viruses; and, in addition, that recently infected mothers are more likely to harbour IFNα-resistant virus than chronically infected mothers. The gene discussed is IFNA1; the disease is infection.